Journal
CURRENT PHARMACEUTICAL DESIGN
Volume 22, Issue 18, Pages 2640-2649Publisher
BENTHAM SCIENCE PUBL LTD
DOI: 10.2174/1381612822666160209152033
Keywords
Type 2 diabetes; mitochondria; reticulum stress; mitochondria; oxidative stress
Categories
Funding
- European Regional Development Fund (ERDF A way to build Europe)
- Ministry of Health of the Valencian Regional Government
- Carlos III Health Institute [CES10/030, CP10/0360, FI14/00125, CD14/00043]
- [PI13/1025]
- [PI12/1984]
- [PI13/0073]
- [CIBERehd CB06/04/0071]
- [PROMETEOII2014/035]
- [UGP-14-93]
- [UGP-14-95]
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It is generally accepted that mitochondrial dysfunction and endoplasmic reticulum (ER) stress are related to insulin resistance and type 2 diabetes. Mitochondria use substrates from lipid and glucose metabolism in order to generate ATP, and when mitochondrial O-2 consumption is decreased due to an altered metabolism there is an increase in reactive oxygen species (ROS) that can impair different types of molecules and cells, especially in beta-cells during type 2 diabetes. Furthermore, the maintenance of ER function in insulin-secreting beta-cells is crucial, and when ER homeostasis is disrupted, the ER develops an unfolded protein response (UPR) in order to maintain the homeostasis of this organelle. However, when homeostasis fails in mitochondria and ER, these organelles can initiate death signalling pathways. New research has suggested that hyperlipidemia and hyperliglucaemia, known as key factors of type 2 diabetes (T2D), disrupt mitochondrial activity and ER homeostasis, thus triggering a disruption of energy metabolism, unresolvable UPR activation and beta-cell death. This review explains the mechanisms of mitochondrial function and ER stress related to the pathological effects of type 2 diabetes in different tissues.
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